期刊
CELL REPORTS
卷 24, 期 11, 页码 2827-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2018.08.024
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资金
- Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan [17H04172, 26115008, 15K15306]
- Takeda Medical Research Foundation
- Japan Foundation for Applied Enzymology
- Takeda Science Foundation
- SENSHIN Medical Research Foundation
- Terumo Foundation
- Manpei Suzuki Diabetes Foundation
- Naito Foundation
- Novartis Foundation
- Japan Society for the Promotion of Science [JSPS] KAKENHI [26893080]
- Uehara Memorial Foundation
- Kowa Life Science Foundation
- Ono Medical Research Foundation
- Nakajima Foundation
- Suzuken Memorial Foundation
- JSPS KAKENHI [16H06244, 17K19648, 16K19531]
- Japan Agency for Medical Research and Development (AMED) [JP17gm5010002]
- Astellas Foundation for Research on Metabolic Disorders
- Bourbon
- TrygFonden
- Danish National Research Foundation [DNRF55]
- Grants-in-Aid for Scientific Research [17H04172, 17K19648, 16K19531, 16H06244, 15K15306, 26893080] Funding Source: KAKEN
Brown adipose tissue (BAT) is a metabolically active organ that contributes to the maintenance of systemic metabolism. The sympathetic nervous system plays important roles in the homeostasis of BAT and promotes its browning and activation. However, the role of other neurotransmitters in BAT homeostasis remains largely unknown. Our metabolomic analyses reveal that gamma-aminobutyric acid (GABA) levels are increased in the interscapular BAT of mice with dietary obesity. We also found a significant increase in GABA-type B receptor subunit 1 (GABA-BR1) in the cell membranes of brown adipocytes of dietary obese mice. When administered to obese mice, GABA induces BAT dysfunction together with systemic metabolic disorder. Conversely, the genetic inactivation or inhibition of GABA-BR1 leads to the re-browning of BAT under conditions of metabolic stress and ameliorated systemic glucose intolerance. These results indicate that the constitutive activation of GABA/GABA-BR1 signaling in obesity promotes BAT dysfunction and systemic metabolic derangement.
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